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血小板衍生的微颗粒在脑梗死大鼠模型中的远程缺血预处理中起作用。

Platelet-derived microparticles are implicated in remote ischemia conditioning in a rat model of cerebral infarction.

机构信息

Key Laboratory of Cardiovascular Disease and Molecular Intervention, State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, China.

出版信息

CNS Neurosci Ther. 2013 Dec;19(12):917-25. doi: 10.1111/cns.12199. Epub 2013 Nov 4.

DOI:10.1111/cns.12199
PMID:24267641
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6493608/
Abstract

AIM

Remote ischemic preconditioning protects against ischemic organ damage by giving short periods of subcritical ischemia to a remote organ. We tested the hypothesis that remote ischemic conditioning can attenuate cerebral stroke in a rat middle cerebral artery occlusion (MCAO) model by microparticles (MPs).

METHODS AND RESULTS

MPs were extracted from healthy rats that underwent hindlimb ischemia-reperfusion preconditioning (RIPC), and were transfused into rats that had undergone MCAO without RIPC. The transfusion resulted in an increase in platelet-derived MPs in blood and reduction in infarction area, confirmed by both 2-3-5-triphenyltetrazolium chloride staining and magnetic resonance imaging, albeit to a lesser degree than RIPC itself. Behavioral tests (modified Neurological Severity Score [mNSS]) were calculated to judge the behavioral change. However, no significant difference was observed after MP transfusion in 24 h or the following consecutive 9 days.

CONCLUSIONS

RIPC induces an increase in MPs, and platelet-derived MPs may confer at least part of the remote protective effect against cerebral ischemic-reperfusion injury.

摘要

目的

通过对远程器官进行短暂的亚临界缺血,远程缺血预处理可防止缺血性器官损伤。我们通过微粒(MPs)测试了这样一个假设,即远程缺血预处理可以减轻大鼠大脑中动脉闭塞(MCAO)模型中的脑卒。

方法和结果

从经历过下肢缺血再灌注预处理(RIPC)的健康大鼠中提取 MPs,并输注到未经历 RIPC 的 MCAO 大鼠中。通过 2-3-5-三苯基氯化四氮唑染色和磁共振成像证实,输注导致血液中血小板衍生的 MPs 增加,梗塞面积减少,但程度低于 RIPC 本身。通过改良神经功能缺损评分(mNSS)计算行为测试来判断行为变化。然而,MP 输注后 24 小时或随后的连续 9 天,观察到的差异没有统计学意义。

结论

RIPC 诱导 MPs 增加,血小板衍生的 MPs 可能至少部分赋予对脑缺血再灌注损伤的远程保护作用。

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本文引用的文献

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Small-size circulating microparticles in acute coronary syndromes: relevance to fibrinolytic status, reparative markers and outcomes.急性冠状动脉综合征中小粒径循环微颗粒:与纤溶状态、修复标志物及预后的相关性。
Atherosclerosis. 2013 Apr;227(2):313-22. doi: 10.1016/j.atherosclerosis.2013.01.028. Epub 2013 Jan 29.
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Transient lack of glucose but not O2 is involved in ischemic postconditioning-induced neuroprotection.短暂性葡萄糖缺乏而非缺氧参与缺血后适应诱导的神经保护作用。
CNS Neurosci Ther. 2013 Jan;19(1):30-7. doi: 10.1111/cns.12033. Epub 2012 Nov 20.
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The role of platelets and their microparticles in rehabilitation of ischemic brain tissue.血小板及其微颗粒在缺血性脑组织修复中的作用。
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A double-edged sword with therapeutic potential: an updated role of autophagy in ischemic cerebral injury.双刃剑的治疗潜力:自噬在缺血性脑损伤中的作用更新。
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6
Ischemic postconditioning diminishes matrix metalloproteinase 9 expression and attenuates loss of the extracellular matrix proteins in rats following middle cerebral artery occlusion and reperfusion.缺血后处理可减少大脑中动脉闭塞再灌注后大鼠基质金属蛋白酶 9 的表达,并减轻细胞外基质蛋白的丢失。
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Microparticle release in remote ischemic conditioning mechanism.远程缺血预处理中微粒的释放机制。
Am J Physiol Heart Circ Physiol. 2012 Oct 1;303(7):H871-7. doi: 10.1152/ajpheart.00102.2012. Epub 2012 Aug 10.
8
Endothelial microparticle uptake in target cells is annexin I/phosphatidylserine receptor dependent and prevents apoptosis.内皮细胞微颗粒被靶细胞摄取依赖于膜联蛋白 I/磷脂酰丝氨酸受体,并能阻止细胞凋亡。
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Platelet microparticles induce angiogenesis and neurogenesis after cerebral ischemia.血小板微粒体诱导脑缺血后血管生成和神经发生。
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Microvesicles derived from endothelial progenitor cells protect the kidney from ischemia-reperfusion injury by microRNA-dependent reprogramming of resident renal cells.内皮祖细胞来源的微小囊泡通过 microRNA 依赖的固有肾细胞重编程来保护肾脏免受缺血再灌注损伤。
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